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1 egulates the quiescent state of the skeletal muscle satellite cell.
2 ll cycle progression to regulate function in muscle satellite cells.
3 maged muscle fibers and within the activated muscle satellite cells.
4 ze to the myogenin promoter in primary adult muscle satellite cells.
5 we show that the growing tail contains many muscle satellite cells.
6 lls" that share several characteristics with muscle satellite cells.
7 ecific, further implicating a defect in FSHD muscle satellite cells.
8 o be the Drosophila equivalent of vertebrate muscle satellite cells.
9 ess that requires activation and division of muscle satellite cells.
10 ted the activation of Pax7-positive skeletal muscle satellite cells and increased its local populatio
14 argely Hh quiescent and that Pax7-expressing muscle satellite cells are not able to give rise to eRMS
15 show that the majority of, if not all, limb muscle satellite cells arise from cells expressing Pax3
17 he Pax7 transcription factor is required for muscle satellite cell biogenesis and specification of th
19 Although mitotically quiescent in mature muscle, satellite cells can be activated to produce myob
20 nomic profiles of preadipocytes and skeletal muscle satellite cells collected from irradiated mice.
21 mportantly, transplanted cells also seed the muscle satellite cell compartment, and engraftment is pr
22 Unexpectedly, expression of Pax3:Fkhr in muscle satellite cells did not produce tumors, but it di
23 and fibro/adipogenic progenitors (FAPs) from muscle; satellite cells did not differentiate into adipo
26 shown concurrent activation and apoptosis of muscle satellite cells following a burn injury in paedia
27 The ongoing activation and recruitment of muscle satellite cells for myofiber regeneration results
29 ogenic program is repressed, suggesting that muscle satellite cells have undergone chondrogenic diffe
32 factor Amphiregulin, which acted directly on muscle satellite cells in vitro and improved muscle repa
33 e results imply that premature senescence of muscle satellite cells is an underlying pathogenic featu
34 nd immunostaining of in vitro differentiated muscle satellite cells isolated from Mkx-null mice revea
35 timulates proliferation of the MM14 skeletal muscle satellite cell line in the absence of exogenously
37 model of replicative senescence, decline in muscle satellite cell-mediated regeneration coincides wi
38 ption factor that plays an essential role in muscle satellite cell (muscle stem cell) differentiation
40 owth defect and a moderately decreased Pax7+ muscle satellite cell pool, phenocopying Pax7 deficiency
41 ly elevated levels of TWEAK, which stimulate muscle satellite cell proliferation and tissue regenerat
44 burn trauma and we propose that an impaired muscle satellite cell response is key in the aetiology o
45 eletal muscle health; however, its effect on muscle satellite cells (SCs) remains largely unknown.
46 ar response after muscle injury, focusing on muscle satellite cells (SCs), inflammatory reaction, fib
47 hese putative stem cells may be identical to muscle satellite cells, some of which lack myogenic regu
48 muscle reveal a marked decrease in quiescent muscle satellite cells suggesting a deregulation of post
50 The stress-induced progression of BMDC to muscle satellite cell to muscle fiber results in a contr
51 s deleted and oncogenic Kras is activated in muscle satellite cells via a Pax7(CreER) driver followin
52 ovel, inducible Pax7-CreER line for tracking muscle satellite cells, we demonstrate the longitudinal
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